Chapter 12
erythrocyte progenitor cells and their differentiation into
mature erythrocytes.
Erythropoietin is normally secreted in small amounts
that stimulate the bone marrow to produce erythrocytes at
a rate adequate to replace the usual loss. The erythropoietin
secretion rate is increased markedly above basal values when
there is a decreased oxygen delivery to the kidneys. Situations
in which this occurs include insuffi cient pumping of blood
by the heart, lung disease, anemia (a decrease in number of
erythrocytes or in hemoglobin concentration), and exposure
to high altitude. As a result of the increase in erythropoietin
secretion, plasma erythropoietin concentration, erythrocyte
production, and the oxygen-carrying capacity of the blood
all increase. Therefore, oxygen delivery to the tissues returns
toward normal (
Figure 12–69
Testosterone, the male sex hormone, also stimulates the
release of erythropoietin. This accounts in part for the higher
hematocrit in men than in women.
As just described,
is defi ned as a decrease in the abil-
ity of the blood to carry oxygen due to (1) a decrease in the
total number of erythrocytes, each having a normal quantity
of hemoglobin, (2) a diminished concentration of hemoglobin
per erythrocyte, or (3) a combination of both. Anemia has a
wide variety of causes, summarized in
Table 12–10
Sickle-cell anemia
is due to a genetic mutation that
alters one amino acid in the hemoglobin chain. At the low
oxygen concentrations existing in many capillaries, the abnor-
mal hemoglobin molecules interact with each other to form
fi berlike structures that distort the erythrocyte membrane and
cause the cell to form sickle shapes or other bizarre forms (a
“sickle” is a crescent-shaped cutting blade). This causes both
the blockage of capillaries, with consequent tissue damage
and pain, and the destruction of the deformed erythrocytes,
with consequent anemia. Sickle-cell anemia is an example of a
disease that is manifested fully only in people homozygous for
the mutated gene (that is, they have two copies of the mutated
gene, one from each parent). In heterozygotes (one mutated
copy and one normal gene), people who are said to have
sickle-cell “trait,” the normal gene codes for normal hemoglo-
bin and the mutated gene for the abnormal hemoglobin. The
erythrocytes in this case contain both types of hemoglobin,
but symptoms are observed only when the oxygen concentra-
tion is unusually low, as at high altitude. The persistence of
the sickle-cell mutation in humans is due to the fact that het-
erozygotes are more resistant to
a blood infection
caused by a protozoan parasite that is spread by mosquitoes
in tropical regions. The mechanisms of this resistance are still
being investigated.
Finally, there also exist conditions in which the prob-
lem is just the opposite of anemia, namely, more erythrocytes
than normal; this is termed
An example, to be
described in Chapter 13, is the polycythemia that occurs in
high-altitude dwellers. In this case, the increased number of
erythrocytes is an adaptive response because it increases the
oxygen-carrying capacity of blood exposed to low oxygen
levels. As discussed earlier, however, raising the hematocrit
increases the viscosity of blood, and thus the existence of poly-
cythemia makes the fl ow of blood through blood vessels more
diffi cult and puts a strain on the heart.
If appropriate dyes are added to a drop of blood, which is then
examined under a microscope, the various classes of leuko-
cytes (
Table 12–11
) are clearly visible (
Figure 12–70
). They
Restoration of O
Blood O
-carrying capacity
Blood Hb concentration
Plasma erythropoietin
delivery to kidneys
Bone marrow
Production of erythrocytes
Erythropoietin secretion
Figure 12–69
Refl ex by which decreased oxygen delivery to the kidneys increases
erythrocyte production via increased erythropoietin secretion.
Table 12–10
Major Causes of Anemia
1. Dietary defi ciencies of iron
ciency anemia
vitamin B
, or folic acid
2. Bone marrow failure due to toxic drugs or cancer
3. Blood loss from the body
leading to iron
defi ciency
4. Inadequate secretion of erythropoietin in kidney disease
5. Excessive destruction of erythrocytes (e.g., sickle-cell
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